Recent research suggests that many of the structural and electrophysiological changes that lead to AF can be attenuated or reversed through treatment with Upstream Therapy targeting the rennin-angiotensin II-aldosterone system (RAAS). Upstream therapy such as angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs) and spironolactone possess antifibrotic properties, in addition, to their more well-known mechanisms of action. Most clinical trial data suggest RAAS inhibition with ACEI or ARB are associated with a lower risk of incident AF in patients with heart failure, but data from hypertension trials have been inconsistent.